Selasa, 29 Juli 2008

Nursing2008 Critical Care

Take a rapid treatment approach to cardiogenic shock

At Penn Presbyterian Medical Center, Philadelphia, Pa., Diane Gorman , Kim Calhoun , Maria Carassco , Donna Niclaus , Mildred Neron, Laura McNally , and Peturah Thompson are staff in the coronary intensive care unit.

Cardiac failure with cardiogenic shock continues to be an ongoing clinical problem.

Cardiogenic shock is a major and frequently fatal complication of a variety of acute and chronic disorders. It is the failure of the heart muscle to effectively pump blood forward, thus a failure to maintain adequate tissue perfusion. Cardiac failure with cardiogenic shock continues to be an ongoing clinical problem. The management of this condition requires a rapid and well-organized treatment approach. 1

The most common cause of cardiogenic shock is acute myocardial infarction (AMI). Timely recognition of cardiogenic shock is essential to provide appropriate interventions.

The incidence of cardiogenic shock ranges from 5% to 10% in patients with AMI. Several multicenter fibrinolytics trials in Europe report a prevalence rate of approximately 7% for cardiogenic shock following AMI. 1 The mortality rate from cardiogenic shock is approximately 50%; recent studies have reported comparable in-hospital mortality rates in the range of 56% to 67%. With the initiation of fibrinolytics, improved interventional procedures, and better medical therapies for heart failure, the mortality rates from cardiogenic shock are expected to continue to decline. 1 We'll use this case study to present signs and symptoms of cardiogenic shock.
Case study

Mr. B., a 48-year-old man, was in a business meeting when he developed severe substernal chest pain, diaphoresis, nausea, and shortness of breath. His colleague called 911 and he was promptly transported to the emergency department. On arrival, Mr. B. continues to complain of chest pain and is noted to be diaphoretic and pale, with cool and mottled extremities. His initial vital signs are heart rate 110 beats/minute, blood pressure 85/50, respiratory rate 28 breaths/minute and labored, and temperature 97.1° F orally. Mr. B. initially is given supplemental oxygen via 100% non-rebreather mask; the cardiac monitor is applied, which shows sinus tachycardia; and I.V. access is obtained. An initial 12-lead electrocardiogram indicates that Mr. B. is having an anteroseptal wall MI. (See ST-elevations in leads V 1 -V 4 suggest acute anteroseptal wall myocardial infarction.) His presenting signs and symptoms suggest that he is in cardiogenic shock, a life-threatening complication of AMI associated with high mortality. Mr. B. needs aggressive treatment to survive this condition.

Figure. ST-elevations in leads V 1 -V 4 suggest acute anteroseptal wall myocardial infarction (ASMI)

Following cardiogenic shock, oxygen cannot be delivered to tissues. 2 Many conditions can lead to cardiogenic shock. (See Other conditions that can lead to cardiogenic shock.)

In AMI, heart muscle (myocardium) dies. Areas of dead myocardium lead to diminished contractility, resulting in reduced ejection fraction (percentage of blood present in the ventricle at end-diastole that is pumped out with each heart beat) and reduced cardiac output. This reduced ventricular emptying increases pressure within the ventricles, resulting in dilation of the ventricles and eventually failure of one or both ventricles, causing hypotension or congestive heart failure. 3 Hemodynamic measurements reveal persistent hypotension, low cardiac output, and high filling pressures. 4
Signs and symptoms

Clinical signs and symptoms that are associated with cardiogenic shock include jugular vein distension, a pathological S 3 or ventricular gallop, and pulmonary edema. Cardiogenic shock is also defined as sustained hypotension (systolic blood pressure less than 90 mm Hg for longer than 30 minutes) and evidence of tissue hypoperfusion with adequate left ventricular filling pressure. 4 Tissue hypoperfusion can be defined or exhibited by such signs as cool extremities; oliguria (urine output less than 30 mL/hour or less than 0.5 mL/kg/hour); or both. 3 Occult tissue hypoperfusion can also be detected by drawing a serum lactic acid level. While a patient may not exhibit low blood pressure initially, a lactic acid value greater than 4 mmol/L can detect organ dysfunction at the cellular level even before the patient becomes hypotensive. 5 This measurement can be a very valuable tool in any type of shock assessment.

Cardiogenic shock signs and symptoms can be related to inadequate cardiac output or related to venous congestion. Inadequate cardiac output leads to hypoperfusion of major organs. Signs of hypoperfusion may present as altered mental status or decreased urine output. Backup of blood into the lungs can be auscultated as pulmonary crackles. As the body attempts to improve oxygenation, the respiratory rate increases. This measurement is verified on arterial blood gas results as hypocapnia and alkalosis (PaCO 2 less than 35 or pH greater than 7.45). As shock progresses, the respiratory system continues to fail and the kidneys also fail as a result of hypoperfusion. Hypercapnia and acidosis ensue and are evident on subsequent arterial blood gas measurements. 2

The skin becomes cool, pale, and clammy as blood is shunted away from the periphery to the vital organs. As blood is shunted away from the skeletal muscles, wasting and lactic acid buildup occur. The shunting of blood away from the gastrointestinal tract causes bowel sounds to decrease and can eventually progress to absent bowel sounds or paralytic ileus. 2 Breathing may become labored as a result of pulmonary congestion as evidenced by course crackles or wheezing. Tachycardia, hypotension, diaphoresis, and poor peripheral pulses may also be present. 3

In our case, Mr. B.'s initial presentation reveals signs of the early compensatory phase of shock. Prompt aggressive medical treatment should occur if Mr. B. is to survive.

In the state of shock, the sympathetic nervous system is responding to a failing heart. Stimulation of the renin-angiotensin-aldosterone system leads to vasoconstriction and sodium and water retention to maintain blood pressure. Cardiac output needs to be maintained sufficiently to perfuse organs. Heart rate and stroke volume (amount of blood pumped out with each ventricular contraction or the difference between the end-diastolic and end-systolic volumes) increase in response to the failing left ventricle.
The hemodynamic principles of cardiogenic shock

A pulmonary artery catheter and arterial line are important tools used in assessing hemodynamics. The pulmonary artery catheter is used to measure the pressures within the heart and the cardiac output. An arterial line is used to monitor blood pressure continuously and can be used to monitor laboratory values, including arterial blood gases.

Cardiac output, measured in liters per minute, is defined as the amount of blood pumped out of the heart per minute. Normal cardiac output values are 4 to 8 L/minute; in cardiogenic shock this value can drop significantly. Cardiac index is a better way of measuring cardiac output based on a person's height and weight or body surface area. A normal cardiac index is 2.5 to 4 L/minute. 2 In a cardiogenic shock state, the body responds by increasing the heart rate or stroke volume or both in an attempt to keep the cardiac output and index within the normal range. However, the increase in heart rate also increases the oxygen demand of already damaged heart muscle. In addition, the increase in heart rate decreases diastolic filling time, which negatively impacts cardiac output even further. The pump continues to fail and cannot keep pace with the increase in volume.

Preload : The degree of stretch and pressure in the myocardium that is produced by blood volume in the ventricles at the end of diastole is termed preload. 2 The central venous pressure or the right atrial pressure reflects right-sided heart preload. The pulmonary artery wedge pressure reflects left-sided heart preload. In a cardiogenic shock state, one or more of these pressures may be greatly decreased or elevated depending on the type of AMI.

Afterload : Afterload is defined as the resistance against which the ventricles have to pump. 2 The components of afterload include systemic vascular resistance, which is the resistance that the left ventricle must pump against, and the pulmonary vascular resistance, which the right ventricle must pump against. Normally, the systemic vascular resistance value ranges from 800 to 1200 dynes/second/cm 5 and the pulmonary vascular resistance value is less than 250 dynes/second/cm 5 . In shock, these values may be significantly elevated because of constriction of the vasculature as the body attempts to respond to sympathetic nervous system stimulation. Mean arterial blood pressure (MAP) is a measurement of end-organ perfusion (normal MAP, 60 to 110 mm Hg). In shock, a value of less than 60 mm Hg is not adequate to maintain organ perfusion. Mean arterial blood pressure is directly affected by cardiac output. As the cardiac output falls, so does MAP. (See Normal and cardiogenic shock hemodynamic values.) Continuously monitoring these values helps clinicians determine adequacy of current interventions.

Table. Normal and cardiogenic shock hemodynamic values

Contractility : Cardiac contractility is the ability of the myocardium to expand and contract to pump blood. It can be indirectly measured by the right and left ventricle stroke work indexes. Poor contractility directly affects cardiac output and decreases stroke volume. In cardiogenic shock, contractility can be manipulated by using a positive inotropic agent. To apply appropriate therapy, it is important for the clinician to recognize changes in hemodynamic values quickly and to have a clear understanding of each of these parameters in relation to the patient's clinical presentation and how they are affected in the shock state.
Available treatments

See The hemodynamic goals of I.V. drug therapy and Treatments and nursing considerations for outlines on specific interventions, benefits, and goals of cardiogenic shock therapy.

Table. Treatments and nursing considerations

Mr. B.'s best chance of recovery relies on rapid percutaneous or surgical revascularization, but there are pharmacologic measures that can optimize his cardiac output to buy time while awaiting revascularization. It is clear that Mr. B. is demonstrating signs of poor cardiac output. He has mottled skin, cool extremities, is hard to arouse, and has poor urinary output. Positive inotropic medication may be needed to increase contractility resulting in increased cardiac output. Inotropes must be used cautiously in patients because they lead to increased myocardial oxygen demand. Increasing contractility and cardiac output in an ischemic heart may increase the incidence of a fatal dysrhythmia. 6 Examples of inotropic drugs include dopamine, dobutamine, and milrinone.

Pulmonary congestion or edema may result in hypoxemia, which can further increase oxygen demand. Mechanical ventilation may be necessary to provide adequate oxygenation. It can also help decrease the work of breathing. Patients who are intubated receive I.V. sedation, which can also aid in decreasing metabolic demands by decreasing anxiety level. Sedation must also be used cautiously, so as not to cause a further drop in blood pressure. Additional considerations include defibrillators and temporary pacing equipment, to treat dysrhythmias such as ventricular tachycardia, ventricular fibrillation, or heart block.

In the treatment of cardiogenic shock, a drug that treats one variable often undermines another. For example, diuretics may be used to decrease preload or lessen pulmonary edema. As a result, hypotension may occur, necessitating the use of vasopressors or I.V. fluids to increase preload. In patients with right ventricular dysfunction, aggressive fluid therapy is often given to increase cardiac output. Diuretics in this case are contraindicated.

Mr. B. is tachycardic to compensate for his decreased stroke volume and hypotension. It is important to avoid an extremely high heart rate because of the increase in oxygen demand; however, in the early stages of AMI it is important to use such medications as beta-blockers to slow the compensatory increase in heart rate if there are no signs or symptoms of acute heart failure.

Antiarrhythmic medications such as amiodarone or lidocaine may be indicated to treat life-threatening ventricular dysrhythmias.

Although decreasing systemic vascular resistance and providing inotropic support are important in the management of cardiogenic shock, maintenance of adequate MAP to prevent end-organ damage is vital. 7 Norepinephrine may be added to the medication regimen to increase MAP, but it may have a negative effect on cardiac output. In cardiogenic shock its use is mainly limited to combination therapy in severe hypotension. 8 No data exist on improving outcomes of patients with cardiogenic shock treated by any catecholamine; however, by monitoring urinary output and calculating cardiac output, assumptions are made that these drugs are supporting the patient's organs and are “buying time” before revascularization and the return of adequate pump function. 6 Any patient admitted with a diagnosis of acute coronary syndromes, including patients in cardiogenic shock, is treated with I.V. anticoagulation (heparin) and aspirin to reduce the progression of the infarct, unless contraindicated.

Table. Hemodynamic effects of drugs

In one study, experts found there was no reduction of in-hospital or long-term mortality for patients treated with fibrinolytics. 9 If there is a possibility that a patient will undergo percutaneous or surgical revascularization, the use of fibrinolytics is not recommended. The aforementioned study, however, noted an improvement in hospital mortality with the use of the glycoprotein IIb-IIIa inhibitor abciximab (ReoPro). 9 It has recently been found to reduce mortality from 40% to 50% down to 18% to 26% in cardiogenic shock treated with stent implantation. 10
Percutaneous coronary intervention

To prevent or limit damage to Mr. B.'s heart muscle, immediate reperfusion of the heart muscle is vital. Percutaneous coronary intervention (PCI) describes a nonsurgical coronary revascularization procedure that relieves the narrowing or obstruction of the coronary artery or arteries to allow more blood and oxygen to be delivered to the heart muscle. In this procedure, a small balloon-tipped catheter inserted into the femoral or brachial artery is advanced to the site of narrowing in the coronary artery. The balloon is then inflated to displace the narrowed lumen of the artery. An intracoronary stent can also be deployed during this procedure.

Several studies and randomized trials have demonstrated the superiority of percutaneous transluminal coronary angioplasty (PTCA) for early reperfusion of patients with AMI, resulting in improved patency rate and clinical outcomes. 11-13 Percutaneous transluminal coronary angioplasty is the preferred reperfusion strategy and is widely used in many institutions in the United States. 11 The American College of Cardiology and the American Heart Association have revised the 2003 PTCA Guidelines, aiming to provide reperfusion of the infarct artery within 90 minutes after arrival to the hospital. These new guidelines also assist in decision making regarding PCI, ensuring patient safety and improving patient quality of care. 4

PTCA does not offer absolute safety to the patient. Emergent and late complications have also been identified with this intervention. One of the most serious complications is abrupt coronary artery occlusion or acute restenosis. This could be a result of tearing of the inner lining of the artery, blood clotting at the balloon site, and constriction of the artery at the balloon site. The introduction of a drug-eluting stent has decreased the incidence of abrupt closures by eliminating the problem of flow-limiting arterial dissection, elastic recoil, and spasm of the artery, enhancing the safety and efficacy of PTCA. 14 The stent remains permanently in place in the artery. (See Intracoronary stent deployment.) 9

Figure. Intracoronary stent deployment

The use of PTCA and stenting improves oxygenation to the heart muscle, decreasing the ensuing complication of an AMI, which is cardiogenic shock. 15
Intra-aortic balloon pump

The use of an intra-aortic balloon pump (IABP) improves coronary artery perfusion and reduces afterload. This mechanical device consists of a 34- to 40-mL balloon catheter, which is placed percutaneously into the patient's aorta just distal to the origin of the subclavian artery and above the renal artery branches. 16 The IABP operates by using counterpulsation therapy. The IABP inflates during ventricular diastole (increasing coronary artery perfusion) and deflates during ventricular systole (decreasing afterload or the resistance against which the heart has to pump). 11 (See The ins and outs of the IABP.) The use of an IABP improves the patient's cardiac output and ejection fraction by increasing coronary artery perfusion, and ultimately increases MAP and end-organ perfusion. The IABP also helps decrease the heart rate (which decreases oxygen consumption) and pulmonary artery pressures, especially pulmonary artery diastolic and wedge pressures, decreasing blood volume and workload of the heart. 11 Mr. B. is a good candidate for IABP therapy because he presented with AMI and is showing signs and symptoms of cardiogenic shock.

Figure. The ins and outs of the IABP
Table. Diagnostic tools

Mr. B. was taken directly to the cardiac catheterization laboratory and underwent PCI with drug-eluting stent placement in the left anterior descending coronary artery. An IABP was placed during the procedure to increase coronary artery perfusion and decrease workload of the heart. He was transferred to the cardiac care unit for further management and monitoring and was discharged 5 days later on appropriate medications.
Prevent complications

Cardiogenic shock is a potential life-threatening complication of AMI. Recognition of early signs and symptoms of cardiogenic shock and rapid interventions enable the nurse and treatment team to prevent complications and assist the patient to recovery.
Other conditions that can lead to cardiogenic shock
Congestive heart failure
Cardiac tamponade
Severe valvular dysfunction
Papillary muscle rupture
Acute pulmonary embolism
Tension pneumothorax
Ventricular septal defect
Aortic dissection
Drug overdose
Cardiac or chest trauma
Severe electrolyte imbalance (hypocalcemia, hypophosphatemia)

Source: Porth CM. Essentials of Pathophysiology: Concepts of Altered Health States. 2nd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2006.

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Journal of Perinatal and Neonatal Nursing

Journal of Perinatal and Neonatal Nursing
April/June 2008
Volume 22 Number 2
Pages 133 - 144

Corresponding Author: gretchen Lawhon, PhD, RN, The Children's Regional Hospital, Cooper University Hospital, One Cooper Plaza, Dorrance Suite 755, Camden, NJ 08103, (
Keywords: developmentally supportive care, individualized, NICU training and education, NIDCAP

The Newborn Individualized Developmental Care and Assessment Program (NIDCAP) was developed from a multidisciplinary study of the preterm infant's behavior, and serves as a guide for the newborn intensive care unit (NICU) professional to provide individualized developmental care. Implementation of the NIDCAP approach has reduced the iatrogenic complications of prematurity and enhanced the infant's neurobehavioral competence. This theory- and evidence-based approach involves formal training and education and requires a multidisciplinary commitment to change within the context of the hospital system. Site assessment and self-assessment of individual trainees initiate the process for a thorough and reflective change in clinical practice within the NICU. The training consists of work sessions with the NIDCAP trainer, interspersed with guided independent neurobehavioral observations. The clinical report interprets the meaning of the infant's observed behavior within the context of the NICU environment, the infant's medical status, and the family concerns in order to best articulate the infant's goals, from which individualized suggestions for care are developed. NIDCAP is a system-wide intervention approach that strives to enhance relationships between infants and families and the professionals who care for them.

There is always the inherent challenge facing healthcare professionals in the newborn intensive care nursery of combining the often-extraordinary technological advances in care of the early born and/or high-risk infant with a sensitive and humane approach that acknowledges and builds on the emerging strength of the infant and family. In 1981–1982, a small pilot research study was done by an infant neuropsychologist with support of a neonatologist and nurse administrator in collaboration with the clinical nurse specialist in the intensive care nursery. 1 The study was conducted to evaluate the effectiveness of attending to the very low-birth-weight preterm infant's behavior as a guide to modification of the environment and clinical approach to care in an effort to reduce iatrogenic effects and enhance the emerging competence of the infant. From this research effort, a clinical observational methodology for the formal naturalistic detailed observation of the infant's behavior before, during, and after caregiving interactions was developed. It was at this point that the Newborn Individualized Developmental Care and Assessment Program (NIDCAP) was created with the goal of teaching other newborn intensive care unit (NICU) professionals this same methodology and thereby enabling them to document and utilize the infant's behavior as a guide to providing care to the premature infant.

In 1982, there was little, if any, observational methodology available to glean the intricate details of the preterm infant's behavior. Als had recently completed her work on the Assessment of Preterm Infant's Behavior (APIB), 2 which provided a direct hands on evaluation of an infant's behavior and was developed from the assessment protocol of the Brazelton Neonatal Behavioral Assessment Scale. 3 The APIB was a culmination of Als's unique conceptualization of the developing human newborn from the simultaneous perspectives of ethology, anthropology, physiology, and psychology. These perspectives were used to articulate subsystem differentiation and integration within the newborn in interaction with the environment. Als cataloged the reliably observable newborn's behavior according to the subsystems of the Synactive Theory. 4 This theory delineates infant's behaviors into 3 major subsystems: (1) the autonomic subsystem (color fluctuations, breathing patterns, and visceral stability); (2) the motor subsystem (body tone, posture, and movement); and (3) the state subsystem (range of available states, state robustness and modulation, and transition from one state to another). 5 Within the infant's state subsystem, the infant's alertness and attentional and interactive ability is assessed as well.

Two categories of behaviors emanate from each of these 3 subsystems, approach/self-regulatory behaviors and stress behaviors. The infant has strategies or behaviors available to him or her to move toward and take in stimuli (approach/self-regulatory behaviors) if the input is appropriate in timing, complexity, and intensity in relation to the infant's thresholds of functioning. Such behaviors might include smooth stable respiration (autonomic subsystem), the resting of the hands upon the chest (motor system), and quietly looking upon the adult's face with invested attention (state subsystem). Conversely, the infant has strategies to move away from or avoid inputs that are too complex or intense or are inappropriately timed. Such behaviors are thought of as stress behaviors. These behaviors may include a color change from a pinkish hue to pale (autonomic system), stretching out of his or her legs and feet away from his or her body (motor subsystem), and/or facial grimacing (state subsystem). Rather than labeling each behavior as always stress or approach/self-regulatory, the meaning of any specific behavior must be interpreted within the context in which it occurs. The infant's self-regulatory ability and success of his or her efforts to maintain or regain balance are assessed across subsystems. One of the most important aspects in understanding the preterm infant's behavior is in the appreciation of his or her level of organization and overall subsystem balance while simultaneously being attuned to the infant's stress threshold. When subtle signs of stress begin to appear (eg, diffuse squirming), the caregiver respectfully and sensitively responds to the infant's signs of disorganization (eg, supporting the infant to maintain his or her arms and legs tucked up close to his or her body through gentle hand containment) to support the infant in maintaining subsystem balance. The sensitive and supportive responses to the infant are the basis for the NIDCAP recommendations for care.

The NIDCAP program grew from the first pilot controlled trial of individualized developmental care conducted by Als. 1 It was during this study that the observational methodology was created (ie, naturalistic observation sheet) and from which the first NIDCAP reports were written. Since then, 9 additional studies have been conducted and form the basic evidence for this approach to care (see Table 1 ). 1,6–15 The original small study 1 consisted of 16 infants who had birth weight less than 1250 g, were under 28 weeks' gestation at birth, and required ventilation within 12 hours for at least 48 hours. A psychologist observed infants in the experimental NIDCAP group before, during, and after caregiving interactions every 10 days throughout hospitalization. The behavioral information was shared with the clinical nurse specialist who met with the primary nurses and together they creatively identified caregiving recommendations that would enhance the development of these infants and families. Control group infants were provided traditional neonatal care. The NIDCAP group showed a statistically significant ( P < .05) reduction of days on ventilator, days requiring supplemental oxygen, days requiring gavage feeding, and improved neurodevelopmental outcome utilizing the APIB at term (44 weeks' corrected age) and significant differences in their development at 3, 6 and 9 months in favor of the comparison infants.

Table 1. Primary NIDCAP research

Additional studies have been conducted using the NIDCAP approach with preterm infants with birth weight less than 1500 g. These studies reported decreases in gavage feeding days, length of hospital stay, need for mechanical ventilation, increased weight gain, head growth, and improved neurodevelopmental outcome for the NIDCAP intervention group. 6–9,11,13 In recent studies of preterm infants (birth weight <1200 g), results in favor of the comparison group (those receiving the NIDCAP approach to care) included reductions in the need for supplemental oxygen and reductions in the severity of bronchopulmonary dysplasia and intraventricular hemorrhage. 10,13,14 These studies also reported decreased days on the ventilator, earlier discharge, and less requirement of gavage feeding as seen in earlier studies. 6,10,11,13,14

Buehler and colleagues 12 conducted a randomized controlled trial of the NIDCAP approach with low-risk healthy preterm infants and a cohort of healthy term infants to demonstrate the effectiveness of this care in a healthy population. As would be expected, because of their initial healthy clinical status, there were no differences in medical outcomes among the groups. However, in evaluating all 36 infants at term with the APIB, the NIDCAP preterm infants were comparable to the full-term infants and both groups demonstrated greater neurobehavioral organization than the control preterm infant group. In terms of their neurophysiological functioning, the full-term infants were significantly better than the NIDCAP preterm infants who were significantly better than the control preterm group, specifically in terms of the frontal and occipital lobe functioning. Both this study and a more recent one by Als and colleagues 15 add a unique finding in demonstrating the efficacy of the NIDCAP approach in the healthy preterm population. The study by Als and colleagues 15 was a randomized controlled NIDCAP study to explore the effect of NIDCAP care on neurobehavior, electrophysiology, and brain structure. The study included 30 infants who were medially low risk, had birth weight of less than 2000 g, and aged between 28 and 33 weeks' gestation. The NIDCAP group infants' weekly NIDCAP observations were supplemented with daily support of the NIDCAP developmental specialist, whereas control group infants received traditional neonatal care. In this medically low-risk population, there were no significant medical differences. These were neither expected nor demonstrated. At term (42 weeks' corrected age), all infants were fully evaluated with the APIB and neurophysiological parameters, including electroencephalogram spectral coherence, magnetic resonance diffusion tensor imaging, and measurements of transverse relaxation time. The NIDCAP group in comparison with the control group demonstrated statistically significant improvement in neurobehavioral functioning, enhanced neurophysiology with greater spectral coherence between left frontal to parietal regions, and enhanced brain structure primarily in the left frontal region. The correlations of the brain structural measures (magnetic resonance imaging) with the brain functional measures (behavioral and spectral coherence) showed that improved behavioral regulation (less intensity and hypersensitivity) was associated with more mature frontal brain structural development. 15 When all infants were examined at 9 months, the NIDCAP group in comparison with the control group demonstrated significantly improved neurodevelopmental outcome.

NIDCAP was established in 1984 to provide education and training in developmental observation for healthcare professionals who cared for high-risk infants and their families on a daily basis. 16 In collaboration with the NICU's multidisciplinary team, it soon became evident that NIDCAP involved more than a specific infant's caregiving approach. NIDCAP required changes in the immediate and extended environment. Caregiving processes needed to change from protocol-driven, crisis-oriented intensive care to a calm and nurturing family-centered environment that acknowledges the infant as the guide or structurer of care.

The primary focus of the NIDCAP training was to observe and interpret preterm infant's behavior. From this observation, an individualized report was developed to enhance the emerging competence of the infant and reduce iatrogenic effects of the NICU environment. This report articulated the infant's goals in striving to achieve greater balance and organization as well as offering specific individualized recommendations for care. NIDCAP suggestions for caregiving may include specific ways to structure the physical environment for both the infant and family. For example, providing greater protection of the infant within the incubator (eg, shielding the incubator with a blanket to protect the infant from the surrounding light, sound, and activity level within the NICU); offering specific recommendations for care that will support the infant in achieving his or her apparent goals (eg, providing a specific position to facilitate the infant to bring his or her hand to mouth); or supporting the family in nurturing their infant along his or her developmental trajectory (eg softly speaking to him or her while hand swaddling). This report was then shared with both the professional and family caregivers.

Successful implementation of the NIDCAP approach to care typically requires a 5-year process. There are 6 key components, which ensure the successful implementation of NIDCAP. These include (1) training a developmental specialist and developmental care nurse educator; (2) ensuring 2 full-time equivalent salaried positions dedicated to these 2 positions; (3) training a multidisciplinary leadership support team; (4) training a core group of the nursing staff representing both day and night shifts; (5) the development of a parent council; and (6) the development of reflective process and continuing education opportunities. 16 NIDCAP level I training involves the behavioral observation and implementation of developmental care whereas level II training consists of consultation with the multidisciplinary staff of the NICU to enhance environment and developmental care implementation on a nursery-wide basis.

Once the decision has been made within the NICU multidisciplinary leadership group to embark on NIDCAP level I training, the first step is a thorough assessment of the current situation. Because this training is a system-wide intervention approach to providing care to the infant and family, the NIDCAP's Site Assessment 17 provides the framework for evaluating the strengths and challenges within a unit and hospital system. The site assessment provides a good process for the leadership group of an NICU to assess the organizational structures that are supportive of the implementation of developmental care and serves as a basis for the consultation and guidance with the NIDCAP trainer. In addition to the assessment of the training site, each identified NIDCAP trainee goes through a similar process of self-assessment and reflection at the initiation of NIDCAP training. The Trainee Self-Assessment 18 provides the starting point for joint reflection and assessment of the opportunities for the individual trainee and a base for guidance and consultation with the NIDCAP trainer. In preparation for NIDCAP level I training, required readings lay the groundwork for the understanding of the theoretical background. Many units accomplish the preparatory readings within the context of a journal club to work together and promote discussion of the information. The NIDCAP trainer collaborates with the training site to formulate the NIDCAP training plan, which typically outlines the next several years of training with a corresponding budget. 19

There are 3 key components to the introductory NIDCAP level I training. These include (1) the theoretical introduction, (2) direct observation in the NICU, and (3) site consultation and guidance with key leadership of the unit and hospital. The theoretical introduction contains an overview of embryological and fetal development, the Synactive Theory with full examples of the observable behaviors, theoretical background of both the APIB and NIDCAP, and the implementation of NIDCAP care in the NICU. In addition, a work session is designed to prepare the NIDCAP trainee for the direct observation in the NICU and includes a full discussion of the behaviors included on the NIDCAP Observation Sheet 20 (see Fig 1 ); a review of the impact of training on the NICU; and opportunities for discussion of support for staff. The second key component is the direct observation in the NICU, which is typically done with 2 trainees and begins with the experience of following the path to the infant from an outside entrance. This provides trainees an orientation to the NICU environment and the specific area of the infant's bedside. The NIDCAP trainer then guides the 2 trainees in a complete observation of an infant before, during, and after a caregiving interaction, using the NIDCAP Observation Sheet . 20 This observation tool was developed for the recording of detailed observations of an infant's naturally occurring behaviors in the NICU. The autonomic subsystem has been placed in the upper 4 blocks of the left column followed by motor behaviors. The right column begins with identified observable states of consciousness within the state subsystem and is followed by the continuation of specific motor behaviors. The lower right column contains attentional/interactional behaviors and ends with an area to record the infant's posture, head position, location, and caregiving events (manipulations) as they are offered to the infant. In addition, space is provided (below the manipulations section) to record the sampling of the infant's physiological data: heart rate and blood oxygen saturations are taken from the monitor, and the respiration rate is counted (for 30 s) and recorded as well. The observation involves a continuous systematic 2-minute time sampling of behavior combined with environment and physiologic data as described above. Each observation sheet allows the recording of 10 minutes of the infant's behavior. The observation is done as a continuous recording and typically includes a minimum of 10 to 20 minutes before the caregiving interaction; during the entire caregiving interaction of the infant (eg, checking vital signs, repositioning, diaper changing, and feeding); and an additional minimum of 10 to 20 minutes following the hands-on caregiving interaction with the infant. This method of observing the infant before, during, and after caregiving provides the comprehensive view of the infant's baseline behavior with his or her response during care and handling and the degree to which he or she is able to settle with varying degrees of support following his or her care.

Figure 1. Observation Sheet.

While the trainee may not yet be able to identify all the infant's behaviors, the trainer highlights the pattern of behavior observed. Following the direct observation, the trainer and trainees discuss the observation and reflect on the experience before formulating a NIDCAP write-up, which includes a description of the environment and the infant's behavior (see Fig 2 ). Together the trainer and trainees glean the necessary clinical and family information from the infant's medical record and use this as the additional context for appreciating the meaning of the infant's observed behavior. From the clinical information, a behavioral summary is written. The infant's goals are formulated and suggestions and recommendations that will support the infant in achieving these goals are developed. In addition, the trainer and trainees review the Profile of the Nursery Environment and of Care Components Template 21 and come to consensus on the quantitative scoring of these components. The Profile scales, of which there are currently 24, measure aspects of the environment and care using a 5-point scale (ie, 1 reflecting a less than optimal example or missed developmental opportunity and 5 representing the highest degree of developmental sensitivity). At the end of this session, the trainer and trainees explore and discuss the trainees' perceived strengths, difficulties, and needs in accomplishing the training goals and then formulate a realistic schedule to accomplish the next training objectives. Site consultation and guidance with the key leadership of the unit and hospital are the third key component. This usually includes the NIDCAP trainees and those who will provide ongoing support. The consultation is very important in clarifying training expectations for the trainees and assisting in the review of the process of change in the unit. It helps build on the working relationship between the NIDCAP trainer and the NICU leadership as well as guide and consult on the organizational planning and evaluation of the NIDCAP process.

Figure 2. Neurobehavioral observation (Newborn Individualized Developmental Care and Assessment Program) report. ( Continues )
Figure 2. ( Continued ) Neurobehavioral observation (Newborn Individualized Developmental Care and Assessment Program) report.

As outlined in the NIDCAP Program Guide , 16 the individual NIDCAP trainee must gain an appreciation of the full 24-hour experience of 3 preterm infants in the NICU, who represent varying levels of acuity. In addition, the trainees are to observe 5 healthy full-term infants to gain a broad perspective of the range of newborn behavior to be observed. The trainees are then expected to conduct observations on a minimum of 15 infants in the NICU, who represent different age ranges and different acuity levels from extremely ill to just preparing to be discharged. Each of these observations is written up. At this point, the NIDCAP trainee sends 1 write-up, reflecting his or her best effort thus far, to the trainer for critical review. Through this process, the trainer evaluates the trainee's level of observational skill and ability to write a NIDCAP report. The quality of the report determines whether the trainee is ready for a formal NIDCAP Bedside Workday and the implementation of the Advanced Practicum.

The NIDCAP workday follows the same training format as the introductory observational training. This session is typically more collaborative in nature because the skill level of the trainee has increased since the first introductory training was initiated. When the NIDCAP trainer returns to a training site for a bedside workday(s), another full site consultation is conducted with the hospital and NICU leadership team. After the NIDCAP Bedside Workday has been completed, the NIDCAP trainee is often ready to begin the Advanced Practicum. 22 This experience provides the NIDCAP trainee the opportunity to practice skills in working collaboratively with the multidisciplinary team and the family during the course of the infant's stay in the NICU. The Advanced Practicum typically consists of weekly observations of a very low-birth-weight infant from admission to discharge, as well as following the infant and family as they transition home. Each observation is followed by a formal write-up. The Advanced Practicum is presented in the form of a bedside binder or Developmental Diary. It contains the formal write-ups as well as entries by the family and care team, photographs, and other items that chronicle the infant's progress. One copy is presented to the family. The second copy is submitted to the trainer. The trainer's copy also includes the trainee's reflective process documentation and the formal evaluations of the usefulness of the trainee's support that have been completed by the family and the key team members. The trainer then reviews and evaluates the trainee's progress and, as deemed appropriate, schedules a NIDCAP reliability session.

The NIDCAP trainer and trainee(s) observe the same infant simultaneously yet independently and compare and discuss their complete write-ups. NIDCAP reliability is judged in terms of completeness of the observation; astuteness in understanding; articulation of the infant's strengths, difficulties, and goals; articulation of the dynamic process of the infant's current developmental issues and coregulatory context of family and NICU environment; conceptual astuteness and effectiveness in formulation of the infant's goals and appropriate recommendations; and the accuracy of the assessment of the environment and care. 16 The NIDCAP reliability session(s) presents another opportunity for the NIDCAP trainer to meet with the hospital and NICU leadership to discuss the accomplishments of the NIDCAP training and potential next steps and plans for further integration of the NIDCAP approach to care with infants and their families. For a summary of the NIDCAP training and education process, please refer to Table 2 . NIDCAP trainers often develop long-lasting relationships with those clinical sites in which they have provided training and remain a consultant and resource over many years.

Table 2. NIDCAP training and education

From the early planning for NIDCAP training in a NICU, the NIDCAP trainer provides guidance and site consultation for the administrative and leadership structure to fully appreciate and sustain the integration of NIDCAP in the NICU. Through the developmental evolution of the NIDCAP program, it soon became obvious that nursery-wide implementation is needed to avoid the ineffectiveness and frustration of isolated NIDCAP trainees who fail to have the support of the unit leadership. Ideally, the NIDCAP trainees, who have achieved reliability, are then recognized as the key professionals who will work with the staff to ensure the integration of developmentally supportive relationship-based care. NIDCAP reliable professionals have typically gained a strong sense of both competence and confidence in their approach to caring for infants and families and should be well utilized in a leadership capacity. For most NIDCAP professionals, there is a much stronger sense of pleasure and pride in their work with infants and families. For the NIDCAP approach to be sustained over time in a unit, there must be an integration of the relationship-based developmental care in the philosophy and mission of the unit. Specific aspects of unit functioning, such as multidisciplinary developmental rounds, provide strong administrative support until the true integration is evident in all aspects of unit operations, including daily medical rounds. Once all patient care policies and procedures reflect the relationship-based developmental approach in caring for infants and families, it no longer is viewed as an adjunct or enhancement of care, but rather the inherent underlying philosophy that is evident in every aspect of our interactions with patients, family members, and one another.

From the first scientific investigation of the NIDCAP approach to care in 1981, this training and education program has evolved to an international nonprofit corporation that was established in 2001. The NIDCAP Federation International, Inc. (NFI) has a mission to provide the highest quality of educational training in the implementation of individualized, developmentally supportive, and family-centered care for infants requiring intensive and special medical care, as well as care and support for the families of these infants. The NFI's mission also advocates and upholds such developmental care standards in practice as well as in research. In support of this mission, the NFI strives to be the leading source for formal training and education; research into the effectiveness of best practices; and providing the vision for the future of appropriate newborn intensive and special care delivery. From the original NIDCAP Center in Boston, Massachusetts, there are now 16 NIDCAP centers in 6 countries (see Table 3 ). For more information about NIDCAP training, please refer to the Web site at: .

Table 3. Newborn Individualized Developmental Care and Assessment Program training centers

1. Als H, Lawhon g, Brown E, et al. Individualized behavioral and environmental care for the very low birth weight preterm infant at high risk for bronchopulmonary dysplasia: neonatal intensive care unit and developmental outcome. Pediatrics . 1986;78(6):1123–1132. [Context Link]

2. Als H, Lester BM, Tronick EZ, Brazelton TB. Toward a research instrument for the assessment of preterm infants' behavior (APIB). In: Fitzgerald HE, Lester BM, Yogman MV, eds. Theory and Research in Behavioral Pediatrics . New York: Plenum Press; 1982:36–53. [Context Link]

3. Brazelton TB, Nugent JK. Neonatal Behavioral Assessment Scale . 3rd ed. Cambridge, UK: Cambridge University Press; 1995. Clinics in Developmental Medicine No. 137. [Context Link]

4. Als H. Toward a Synactive Theory of development: promise for the assessment of infant individuality. Infant Ment Health J . 1982;3(4):229–243. [Context Link]

5. Als H. Reading the premature infant. In: Goldson E, ed. Developmental Interventions in the Neonatal Intensive Care Nursery. New York: Oxford University Press; 1999:18–85. [Context Link]

6. Becker PT, Grunwald PC, Moorman J, Stuhr S. Outcomes of developmentally supportive nursing care for very-low-birth-weight infants. Nurs Res . 1991;40:150–155. [Context Link]

7. Stevens B, Petryshen P, Hawkins J, Smith B, Taylor P. Developmental versus conventional care: a comparison of clinical outcomes for very low birth weight infants. Can J Nurs Res. 1996;28:97–113. [Context Link]

8. Westrup B, Kleberg A, Wallin L, Lagercrantz H, Wikblad K, Stjernqvist K. Evaluation of the Newborn Individualized Developmental Care and Assessment Program (NIDCAP®) in a Swedish setting. Prenat Neonatal Med. 1997;2:366–375. [Context Link]

9. Kleberg A, Westrup B, Stjernqvist K. Developmental outcome, child behavior and mother-child interaction at 3 years of age following Newborn Individualized Developmental Care and Intervention Program (NIDCAP) intervention. Early Hum Dev. 2000;60:123–135. [Context Link]

10. Als H, Lawhon g, Duffy FH, McAnulty GB, Gibes-Grossman R, Blickman JG. Individualized developmental care for the very-low-birth-weight infant: medical and neurofunctional effects. JAMA . 1994;272:853–858. [Context Link]

11. Fleisher BF, VandenBerg KA, Constantinou J, et al. Individualized developmental care for very-low-birth-weight premature infants. Clin Pediatr . 1995;34:523–529. [Context Link]

12. Buehler, DM, Als H, Duffy FH, McAnulty GB, Liederman J. Effectiveness of individualized developmental care for low-risk preterm infants: behavioral and electrophysiological evidence. Pediatrics . 1995;96:923–932. [Context Link]

13. Westrup B, Kleberg A, von Eichwald K, Stjernqvist K, Lagercrantz H. A randomized controlled trial to evaluate the effects of the Newborn Individualized Developmental Care and Assessment Program in a Swedish setting. Pediatrics. 2000;105(1):66–72. [Context Link]

14. Als H, Gilkerson L, Duffy FH, et al. A three-center randomized controlled trial of individualized developmental care for very low birth weight preterm infants: medical, neurodevelopmental, parenting and caregiving effects. J Dev Behav Pediatr. 2003;24:399–408. [Context Link]

15. Als H, Duffy FH, McAnulty GB, et al. Early experience alters brain function and structure. Pediatrics . 2004;113:846–857. [Context Link]

16. Als H. Program Guide: Newborn Individualized Developmental Care and Assessment Program (NIDCAP): An Education and Training Program for Health Care Professionals. Rev ed. Boston, MA: NIDCAP Federation International Inc; 2006. [Context Link]

17. Als H. Site Assessment. Rev ed. Boston, MA: NIDCAP Federation International Inc; 2006. [Context Link]

18. Als H. Trainee Self-Assessment. Rev ed. Boston, MA: NIDCAP Federation International Inc; 2006. [Context Link]

19. Als H. Cost-Effectiveness Analysis of Developmental Care (NIDCAP) in the Newborn Intensive Care Unit (NICU). Rev ed. Boston, MA: NIDCAP Federation International Inc; 2006. [Context Link]

20. Als H. NIDCAP Observation Sheet . Rev ed. Boston, MA: NIDCAP Federation International Inc; 2001. [Context Link]

21. Als H, Buehler D, Kerr D, Feinberg E, Gilkerson L. Profile of the Nursery Environment and of Care Components Template Manual, Part 1. Rev ed. Boston, MA: NIDCAP Federation International Inc; 2006. [Context Link]

22. Als H. Guidelines for Advanced Practicum: Following an Infant and Family From Admission to Discharge and Transition to the Home. Rev ed. Boston, MA: NIDCAP Federation International Inc; 2006. [Context Link]

Key words: developmentally supportive care; individualized; NICU training and education; NIDCAP

Journal of Cardiopulmonary Rehabilitation & Prevention

Journal of Cardiopulmonary Rehabilitation & Prevention
May/June 2008
Volume 28 Number 3
Pages 180 - 186

Journal of Cardiopulmonary Rehabilitation and Prevention
Corresponding Author: Ray W. Squires, PhD, Mayo Clinic, Division of Cardiovascular Diseases and Internal Medicine, Gonda 5-318, 200 First St SW, Rochester, MN 55905 (
Keywords: cardiac rehabilitation, long-term disease management

PURPOSE: Randomized-clinical trials have demonstrated the benefits of disease management for patients with coronary disease. It is not known if long-term disease management in routine clinical practice provided by cardiac rehabilitation (CR) program staff is possible. The goal of this study was to evaluate the feasibility and clinical benefits of a 3-year disease-management program in the setting of an outpatient CR facility.

METHODS : Consecutive patients ( n = 503) referred to CR and who were available for long-term follow-up served as subjects. After a phase II CR program, disease managers assessed secondary-prevention goals every 3 to 6 months via face-to-face meetings with each patient. Outcome measures included use of cardioprotective medications, coronary risk factors, amount of habitual exercise training, and all-cause mortality.

RESULTS : At 3 years, aspirin usage was 91%, statin usage 91%, [beta]-blocker usage 78%, and angiotensin-converting enzyme inhibitor usage 76%. Low-density lipoprotein cholesterol was 90 ± 23 mg/dL, systolic blood pressure was 126 ± 19 mm Hg, and body mass index was 29.0 ± 5.1 kg/m 2 . Exercise training averaged 139 ± 123 minutes per week. Annual mortality was 1.9%. There were no differences ( P > .05) in medication usage or low-density lipoprotein cholesterol for men versus women, or for age below 65 years versus age 65 years or greater.

CONCLUSIONS: Long-term disease management of patients with coronary disease in routine clinical practice by CR program staff is feasible and effective in achieving and maintaining secondary-prevention goals. Overweight remains a prevalent and persistent risk factor. We advocate expansion of CR programs into long-term coronary disease-management programs.

Traditional cardiac rehabilitation (CR) programs in the United States include up to 36 sessions of supervised exercise, risk factor education, and counseling over a 3-month period of time. However, long-term adherence to blood lipid–improving medications remains problematic even for patients who participate in traditional CR. 1 In routine clinical practice, there is a continually diminishing level of adherence to treatment recommendations including medications (eg, aspirin and antihypertensives) and lifestyle factors such as regular exercise. 2,3 For the state of Minnesota in the year 2004, only 38% of patients with coronary heart disease received optimal care for secondary prevention defined as a low-density lipoprotein (LDL) cholesterol < 100 mg/dL, blood pressure less than 140/90 mm Hg, daily aspirin, and no smoking. 4

In 1987, we described a long-term program to control risk factors in patients who had completed a phase II outpatient CR program. 5 With this approach, patients periodically returned to the CR program to have face-to-face meetings with nonphysicians (case managers) in order to review all aspects of secondary prevention. Subsequently, investigators from Stanford University demonstrated in 2 separate studies that it was possible to achieve improved risk-factor control, reduced angiographic progression of disease, and decreased clinical events for patients who were randomized to nurse case management for 1 to 4 years versus usual care provided by physicians. 6,7 Recently, systems for longitudinal care for patients with chronic diseases (case management) have been renamed as “disease-management” programs. 8

A concern regarding randomized trials of lifestyle factors and compliance with medical treatment is the potential problem of subject recruitment bias. Patients who meet inclusion criteria for trials and who agree to be randomized may be inherently different from the typical patient in routine clinical practice. The results from randomized trials may not be absolutely applicable to the general population of patients with coronary disease. Another concern is the feasibility of applying, in routine clinical practice, the well-developed disease-management systems employed in the randomized trials. Therefore, the purpose of this project was to determine the feasibility and clinical benefits of long-term (3 years) disease management of patients with coronary disease in routine clinical practice utilizing CR program staff.

The study design was a retrospective analysis of 503 consecutive patients who were referred to and who agreed to participate in outpatient CR in 1999 and 2000. All had suffered an acute-cardiac event including acute myocardial infarction, coronary bypass surgery, and/or percutaneous coronary revascularization. The only exclusion criterion was unavailability for long-term disease management. Of the 605 patients who started outpatient CR in 1999 and 2000, 83% (503 of 605 patients) were available for long-term follow-up. Advanced age was not an exclusion criterion and 54% of the patients were at least 65 years of age. Patient characteristics are provided in Table 1 . Women were slightly older than men (69 ± 12 years vs 65 ± 11 years, P < .01).


Outpatient CR (phase II) began within 1 to 2 weeks after hospital discharge. Program components included 1 to 3 supervised exercise sessions per week (aerobic, strengthening, and flexibility exercises) plus unsupervised “home” exercise as well as group educational meetings. The length of the phase II program ranged from 2 to 8 weeks. Patients participated in 13 ± 7 supervised exercise sessions during the phase II cardiac-rehabilitation program. At the beginning and at the end of phase II, patients met face-to-face with disease managers (PhD-level exercise physiologists or registered nurses). Subsequently, patients met with their disease manager every 3 to 6 months for 3 years. A small minority of patients (6%) continued to exercise in a supervised phase III-IV type program for more than 6 months.

The goal of the disease manager was to optimize secondary-prevention efforts. At each meeting, the following factors were addressed:
* Measured variables : blood lipids, blood pressure, and body weight.
* Patient report variables : tobacco use, cardiac medications, exercise and physical activity, nutrition (assisted by registered dietitians), and cardiopulmonary symptoms.

Physicians were readily accessible for medical decision-making purposes, including adjustment of cardioprotective medications. Treatment of diabetes was deferred to the patients' primary healthcare providers. Communication with the primary and other healthcare providers was accomplished via an electronic medical record. American Heart Association (AHA) guidelines for secondary prevention served as the goals for disease management. 9 We were more aggressive than these guidelines in one respect: we recommended statin medications in all subjects unless intolerance was present.

Follow-up appointments with disease managers were scheduled through the existing institutional advance-appointment system according to the instructions of the disease manager. Standard appointment letters were mailed to the patient's home address. A telephone number was provided if patients needed to reschedule their appointment. Patients who missed their appointment were contacted by the appointment office staff. Patients and/or their insurance plans were billed for the laboratory tests and consultations by our institutional business office. Blood lipids were measured in the institution's clinical laboratory in the morning after a 12-hour fast. Laboratory results were available when the patient was seen in consultation, usually later the same day or the next day. Appointments were scheduled within the normal business hours of 8 AM to 5 PM, Monday through Friday. The face-to-face time required for each consultation was approximately 20 to 30 minutes. Risk factors, medications, symptoms, and exercise habits were addressed and discussed in detail. The data were collected on paper forms and transferred to a database. One or 2 PhD-level exercise physiologists and 1 registered nurse saw patients in consultation each day.

The AHA recently acknowledged that disease-management programs are widely heterogeneous and lack a common definition. 8 The AHA has recommended an 8-point taxonomic system to facilitate comparisons of different disease-management programs and to identify specific factors associated with success. Table 2 contains the AHA classification factors with our study's specific components.


The following outcome measures were assessed after 3 years of disease management:
1. Appropriate use of cardioprotective medications: aspirin and statins for all patients; [beta]-blockers for patients with myocardial infarction as the index event; and angiotensin-converting enzyme inhibitors or receptor blockers for patients with left ventricular ejection fractions below 40%.
2. Selected coronary risk factors (AHA 9 risk factors minus hemoglobin A1c in diabetics): blood lipids, blood pressure, smoking, and body mass index (BMI).
3. Amount of regular exercise training.
4. All-cause mortality.

Comparison of selected continuous variables was accomplished using a 2-tailed t test. The chi-square test was used for nominal variables. The McNemar test was used for comparison of the percentage of patients at the AHA risk-factor goals at years 1 and 3 of disease management. SAS software (version 9.1 for Windows, SAS Institute, Cary, North Carolina) was used for the analysis and a P < .05 was selected for statistical significance. Descriptive statistics were calculated as the mean ± SD.

During the 3 years of follow-up, the total number of face-to-face meetings of disease managers with each patient averaged 6.9 ± 2.1. The total number of disease-management visits per workday averaged 4.6.

After 3 years of disease-management efforts, appropriate usage of cardioprotective medications was as follows for the entire cohort of patients: aspirin 91%; statins 91%; [beta]-blockers 78%; and angiotensin-converting enzyme inhibitors or receptor blockers 76%. With the exception of BMI, coronary risk factors were reasonably controlled: total cholesterol, 164 ± 29 mg/dL; high-density lipoprotein (HDL) cholesterol, 46 ± 11 mg/dL; LDL cholesterol, 90 ± 23 mg(dL; triglycerides, 145 ± 74 mg/dL; systolic blood pressure, 126 ± 19 mm Hg; diastolic blood pressure, 70 ± 11 mm Hg; smoking, 45 patients (9%); and BMI, 29.0 ± 5.1 kg/m 2 . The amount of habitual exercise training averaged 139 ± 123 minutes per week.

Medication usage and coronary risk factors after 1 and 3 years of disease management are shown in Table 3 . Medication usage and most risk-factor values were similar at both time points. Diastolic blood pressure was minimally lower at 3 years. BMI was higher at 3 years by approximately 1 kg/m 2 .


Figure 1 shows the percentage of patients achieving the AHA risk-factor goals after 1 and 3 years of follow-up. There was a significant increase in the achievement of the LDL cholesterol goal from year 1 to year 3 (69% vs 74%, P = .03). At 3 years, a favorable percentage of patients achieved the goals for not smoking (95%), systolic (75%), diastolic (95%), and both blood pressures (73%). After 3 years of disease management, 48% of patients were not smoking and were at goal for both systolic and diastolic blood pressures and for LDL cholesterol. Fifty-seven percent of patients achieved the physical activity goal at year 3. The percentage of patients at the goal for BMI was extremely poor and decreased from year 1 to year 3 (21% vs 17%, P = .02).

Figure 1. Percentage of patients achieving the American Heart Association risk factor goals for persons with atherosclerotic cardiovascular disease 9 at year 1 and year 3 of follow-up.Abbreviations: BMI, body mass index, 18.5–24.9 kg/m 2 ; DBP, diastolic blood pressure < 90 mm Hg; LDL-C, low-density lipoprotein cholesterol < 100 mg/dL; physical activity, >120 min/wk; SBP, systolic blood pressure < 140 mm Hg; SBP and DBP, both systolic and diastolic blood pressures < 140/90.

As shown in Table 4 , cardioprotective medication use was similar for men and women at 3 years. Women had higher total cholesterol level, HDL cholesterol level, triglycerides, and systolic blood pressure. Men exercised more minutes per week than did women. LDL cholesterol, and BMI were similar for men and women.


There were no significant differences in medication usage, exercise training amount, or LDL cholesterol level for younger patients versus older patients at 3 years ( Table 4 ). Older patients had higher HDL cholesterol and lower triglycerides, diastolic blood pressure, and BMI.

Over the 3 years of the intervention in 503 subjects, there were 29 deaths (25 in men and 4 in women) yielding an annual all-cause mortality of 1.9%. This compares favorably to the Centers for Disease Control and Prevention's expected annual mortality of 1.6% for average Americans, in the general population, of similar ages as our patients. 10 Annual mortality over 3 years for the 102 patients who enrolled in CR, but who were not available for disease management, was 6.5%.

The major finding of the current study was that a 3-year coronary disease-management program for a large cohort of patients in routine clinical practice using CR staff was both feasible and generally effective in assisting patients in secondary prevention. Patients, in general, continued to take aspirin, angiotensin-converting enzyme inhibitors or receptor blockers, [beta]-blockers, and statins, as indicated for their clinical status. A favorable percentage of patients achieved the AHA goals for most risk factors. Unfortunately, an excessive BMI remained a persistent and prevalent risk factor. All-cause mortality was low and compared favorably to the expected death rate for average Americans of the same age. Primary healthcare providers were provided ongoing feedback on their patients' performance and the program was well accepted by them.

The benefits of disease-management programs for coronary heart disease patients were established in 1994 with the publication of 2 groundbreaking randomized trials. Haskell et al 6 randomized 274 patients with coronary artery disease to usual care or risk-factor management directed by registered nurses with physician support. Patients in the risk-factor management group had less angiographic progression of their disease and fewer hospitalizations than did the usual care group. DeBusk et al 7 randomized 535 patients with myocardial infarction to usual care or registered nurse disease management. After 1 year, intervention patients exhibited a better smoking cessation rate, lower LDL cholesterol, and a better exercise capacity than usual care subjects.

Results from the present study compare favorably to contemporary-randomized trials with CR-type interventions lasting at least 1 year. After a 4-month standard CR program, the extensive lifestyle management trial randomized coronary heart disease patients to usual care versus risk-factor intervention. 11,12 Of the population of CR graduates who were screened for the study, only 29% were randomized. After 1 year, there was a nonsignificant trend in favor of risk-factor intervention in reduction of a global risk score. The authors speculated that the lack of difference between the usual care and intervention groups might have resulted from self-selection bias (willingness to participate may indicate heightened health consciousness).

Patients with a history of an acute-coronary event underwent baseline testing and subsequent randomization to either usual care or risk-factor intervention in the Vestfold Heartcare Study. 13 After 2 years, intervention subjects had a better diet, were less likely to smoke, and performed more regular exercise than did usual care subjects. Aspirin, [beta]-blocker, and statin medication usage were similar for both groups. Intervention subjects experienced a 22% reduction in estimated relative coronary risk according to the West of Scotland Coronary Prevention Study algorithm.

Reid et al 14 randomized coronary patients to a standard 3-month versus a prolonged 12-month CR program. At 1 year, there were no significant differences between the 2 groups for risk factors, exercise capacity, or cardioprotective medication usage. The authors speculated that the lack of differences between the 2 study groups may have been due to insufficient differences in the interventions, baseline differences between groups (more patients with angina and more current smokers in the prolonged rehabilitation group), or that periodic outcome assessment for both groups may have constituted a form of intervention that contributed to improved secondary prevention in both groups.

The GOSPEL study, 15 a large randomized trial involving coronary patients carried out in 78 CR centers in Italy, was published in abstract form. After completion of a standard CR program, patients were randomized to usual care versus an intensive approach for 3 years. After 3 years, the intensive group exhibited better lifestyle habits, better adherence to cardioprotective medications, and a 12% lower combined endpoint of cardiac death, recurrent myocardial infarction, stroke, revascularization, heart failure, and angina pectoris.

Our results were similar to those from trials utilizing nurse disease-management approaches in multisite medical practices without a specific CR program. Murchie et al 16 reported results from a randomized trial of nurse-directed secondary-prevention programs in general medical practices. Patients with coronary disease were randomized to either usual care versus secondary prevention. After 1 year, subjects in the secondary-prevention group were better when compared with usual care in terms of medication use (eg, aspirin use: 81% vs 66%), blood pressure, blood lipids, exercise, and diet. The groups were similar in smoking rates. Annual total mortality was lower for secondary prevention than for usual care (3.1% vs 4.0%, P < .05) after 4 years of observation.

The recently published COURAGE trial was a multicenter study of patients with angiographic coronary artery disease and evidence of myocardial ischemia during stress testing. 17 Patients were randomized to percutaneous coronary intervention and intensive secondary prevention versus intensive secondary prevention only. Percutaneous intervention did not reduce the risk of death, myocardial infarction, or other major cardiovascular events when compared with intensive secondary prevention only. After 3 years, the same length of intervention as in the present study, annual all-cause mortality was 1.7% versus 1.9% in the present study. With the exception of lower LDL cholesterol in COURAGE, medication usage and other risk factors were similar to those in our study, although the intensity of intervention was greater in COURAGE than in the present study (more frequent clinical visits, lower LDL-cholesterol goal). Table 5 provides summary data from contemporary clinical trials compared with the present study.


In light of these randomized-controlled trials, we believe that our study provides new and important information regarding the role of CR in long-term secondary prevention. The disease-management intervention used in the current study was part of the routine clinical work for the CR staff and was not difficult to develop and implement. It did require physician support and guidance, although the amount of time required of physicians was minimal. We have demonstrated that 3 years of intervention in routine clinical practice was generally effective in achieving secondary-prevention goals. In our study, as well as in many of the randomized trials, overweight appears to be the most difficult modifiable risk factor in terms of achieving long-term control.

Our study has several limitations. Exercise training and medication usage was determined via self-report. There were no baseline data on medications and risk factors. We did not have data on the frequency of change in medications or medication dosage. We did not have quantifiable data regarding recurrent hospitalizations and dietary or psychosocial variables. The study was a retrospective analysis and no contemporary control group was available for comparison. Patients were willing to participate in long-term disease-management activities and this may have introduced selection bias, although a high percentage of patients participated in disease management (83%). The 17% of patients who enrolled in CR, but were not available for disease management, experienced a 3.4-fold higher annual mortality than subjects in disease management. However, these patients may have been different in important characteristics than disease-management participants and should not be considered an adequate control group. Our program is somewhat unique. It is the only CR program in the city. We are part of a large group practice that facilitates a high enrollment rate of eligible patients and facilitates follow-up. 18 The results may not be applicable to patients who choose not to enroll in CR programs. We have previously reported that such patients tend to be older and sicker than are the participants in our program and are more likely to be female. 18

In summary, long-term disease management of typical patients with coronary disease in routine clinical practice by CR program staff is feasible and effective in achieving and maintaining secondary-prevention goals. We advocate expansion of CR into long-term coronary disease-management programs.

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Kamis, 19 Juni 2008



Pokok bahasan : Rokok

Sub pokok bahasan : Bahaya rokok terhadap tubuh

Sasaran : Masyarakat dusun Kembaran Rt:01/ Rw: 01 Yogyakarta

Target : Pengguna rokok

Waktu : 30 menit

Hari/tanggal : Minggu/ 8 juni 2008

Tempat : Balai desa Dusun Kembaran

Penyuluh :Mahasiswa tahap profesi perawat STIKES Surya Global Yogyakarta

Latar Belakang

Rokok adalah silinder dari kertas berukuran panjang antara 70 hingga 120 mm (bervariasi tergantung negara) dengan diameter sekitar 10 mm yang berisi daun-daun tembakau yang telah dicacah. Rokok dibakar pada salah satu ujungnya dan dibiarkan membara agar asapnya dapat dihirup lewat mulut pada ujung lain.

Rokok biasanya dijual dalam bungkusan berbentuk kotak atau kemasan kertas yang dapat dimasukkan dengan mudah ke dalam kantong. Sejak beberapa tahun terakhir, bungkusan-bungkusan tersebut juga umumnya disertai pesan kesehatan yang memperingatkan perokok akan bahaya kesehatan yang dapat ditimbulkan dari merokok, misalnya kanker paru-paru atau serangan jantung(walapun pada kenyataanya itu hanya tinggal hiasan, jarang sekali dipatuhi).

Manusia di dunia yang merokok untuk pertama kalinya adalah suku bangsa Indian di Amerika, untuk keperluan ritual seperti memuja dewa atau roh. Pada abad 16, Ketika bangsa Eropa menemukan benua Amerika, sebagian dari para penjelajah Eropa itu ikut mencoba-coba menghisap rokok dan kemudian membawa tembakau ke Eropa. Kemudian kebiasaan merokok mulai muncul di kalangan bangsawan Eropa. Tapi berbeda dengan bangsa Indian yang merokok untuk keperluan ritual, di Eropa orang merokok hanya untuk kesenangan semata-mata. Abad 17 para pedagang Spanyol masuk ke Turki dan saat itu kebiasaan merokok mulai masuk negara-negara Islam.

Telah banyak riset yang membuktikan bahwa rokok sangat menyebabkan kecanduan, disamping menyebabkan banyak tipe kanker, penyakit jantung, penyakit pernapasan, penyakit pencernaan, dan efek buruk bagi kelahiran.

Tujuan Intruksional Umum

Setelah mendapatkan penyuluhan selama 30 menit tentang bahaya rokok terhadap tubuh, peserta penyuluhan masyarakat dusun kembaran mengerti dampak menggunakan atau mengkonsumsi rokok.

Tujuan Intuksional Khusus

Setelah mendapatkan penyuluhan satu kali diharapkan peserta penyuluhan mampu:

1. Memahami bahaya rokok bagi tubuh

2. Mengerti kandungan atau racun yang terdapat dalam rokok

3. Mengurangi dalam mengkonsumsi rokok

4. Berhenti mengkonsumsi rokok

Stategi Pelaksanaan

1. Metode

a. Ceramah dan tanya jawab

2. Media

a. Pamflet

3. Waktu dan tempat

a. Jam 8 pagi tanggal 8 juni 2008 di Balai Desa Kembaran

4. Garis besar materi

a. Pengertian rokok

b. Kandungan rokok

c. Jenis-jenis rokok

d. Tipe rokok

e. Bahaya rokok

f. Upaya pencegahan

g. Kesimpulan

Proses Pelaksanaan



Respon masyarakat




a. Penyampaian salam

b. Perkenalan

c. Menjelaskan topic penyuluhan

d. Menjelaskan tujuan

e. Menjelaskan waktu pelaksanaan

a. Membalas salam

b. Memperhatikan

c. Memperhatikan

d. Memperhatikan

e. Memperhatikan

10 menit


Penyampaian materi

1. Materi

a. Pengertian rokok

b. Kandungan rokok

c. Jenis-jenis rokok

d. Tipe rokok

e. Bahaya rokok

f. Upaya pencegahan

g. Kesimpulan

2. Memberikan kesempatan untuk bertanya

3. Menjawab pertanyaan peserta

1. Memperhatikan penjelasan dan mencermati materi

2. Bertanya

3. Memperhatikan jawaban

45 menit



a. Menyimpulkan hasil penyuluhan

b. Mengahiri dengan salam

a. Memperhatikan

b. Menjawab salam

5 menit

Setting Tempat

Duduk berhadapan antara penyuluh dengan peserta penyuluhan


1. Pendahuluan

2. Penyampaian materi

3. Penutup

Kriteria Evaluasi

Menanyakan pada peserta penyuluhan tentang:

1. Pengertian rokok

2. Kandungan rokok

3. Jenis-jenis rokok

4. Tipe rokok

5. Bahaya rokok

6. Upaya pencegahan


1. Pengertian Rokok

Rokok merupakan salah satu zat adiktif yang bila digunakan mengakibatkan bahaya kesehatan bagi diri sendiri maupun masyarakat, oleh karena itu diperlukan berbagai kegiatan pengamanan rokok bagi kesehatan

Rokok adalah hasil olahan tembakau terbungkus termasuk cerutu atau bentuk lainnya yang mengandung nikotin dan tar dengan atau tanpa bahan tambahan.

2. Kandungan Rokok

Setiap batang rokok yang dinyalakan akan mengeluarkan lebih 4 000 bahan kimia beracun yang membahayakan dan boleh membawa maut. Dengan ini setiap sedutan itu menyerupai satu sedutan maut. Di antara kandungan asap rokok termasuklah bahan radioaktif (polonium-201) dan bahan-bahan yang digunakan di dalam cat (acetone), pencuci lantai (ammonia), ubat gegat (naphthalene), racun serangga (DDT), racun anai-anai (arsenic), gas beracun (hydrogen cyanide) yang digunakan di “kamar gas maut” bagi pesalah yang menjalani hukuman mati, dan banyak lagi. Bagaimanapun, racun paling penting adalah Tar, Nikotin dan karbon monoksida.

Tar mengandung sekurang-kurangnya 43 bahan kimia yang diketahui menjadi penyebab kanker (karsinogen)..

Nikotin turut menjadi puncak utama risiko serangan penyakit jantung dan strok. Hampir satu perempat mangsa penyakit jantung adalah hasil puncak dari tabiat merokok. Di Malaysia, sakit jantung merupakan menyebab utama kematian sementara strok adalah pembunuh yang keempat.

Karbon Monoksida pula adalah gas beracun yang biasanya dikeluarkan oleh kenderaan. Apabila racun rokok itu memasuki tubuh manusia ataupun hewan, yang akan membawa kerusakkan pada setiap organ, yaitu bermula dari hidung, mulut, tekak, saluran pernafasan, paru-paru, saluran penghazaman, saluran darah, jantung, organ pembiakan, sehinggalah ke saluran kencing dan pundi kencing, yaitu apabila sebahagian dari racun-racun itu dikeluarkan dari badan.

3. Jenis-Jenis Rokok

Rokok dibedakan menjadi beberapa jenis. Pembedaan ini didasarkan atas bahan pembungkus rokok, bahan baku atau isi rokok, proses pembuatan rokok, dan penggunaan filter pada rokok.

Rokok berdasarkan bahan pembungkus.

  • Klobot: rokok yang bahan pembungkusnya berupa daun jagung.
  • Kawung: rokok yang bahan pembungkusnya berupa daun aren.
  • Sigaret: rokok yang bahan pembungkusnya berupa kertas
  • Cerutu: rokok yang bahan pembungkusnya berupa daun tembakau.

Rokok berdasarkan bahan baku atau isi.

  • Rokok Putih: rokok yang bahan baku atau isinya hanya daun tembakau yang diberi saus untuk mendapatkan efek rasa dan aroma tertentu.
  • Rokok Kretek: rokok yang bahan baku atau isinya berupa daun tembakau dan cengkeh yang diberi saus untuk mendapatkan efek rasa dan aroma tertentu.

Rokok Klembak: rokok yang bahan baku atau isinya berupa daun tembakau, cengkeh, dan menyan yang diberi saus untuk mendapatkan efek rasa dan aroma tertentu.

Rokok berdasarkan proses pembuatannya.

Rokok berdasarkan penggunaan filter.

Merek-merek rokok yang terkenal

4. Tipe Perokok

Mereka yang dikatakan perokok sangat berat adalah bila mengkonsumsi rokok lebih dari 31 batang perhari dan selang merokoknya lima menit setelah bangun pagi. Perokok berat merokok sekitar 21-30 batang sehari dengan selang waktu sejak bangun pagi berkisar antara 6 - 30 menit. Perokok sedang menghabiskan rokok 11 – 21 batang dengan selang waktu 31-60 menit setelah bangun pagi. Perokok ringan menghabiskan rokok sekitar 10 batang dengan selang waktu 60 menit dari bangun pagi.

Ada 4 tipe perilaku merokok adalah :

1. Tipe perokok yang dipengaruhi oleh perasaan positif. Dengan merokok seseorang merasakan penambahan rasa yang positif. menambahkan ada 3 sub tipe ini :

a. Perilaku merokok hanya untuk menambah atau meningkatkan kenikmatan yang sudah didapat, misalnya merokok setelah minum kopi atau makan.

b. Perilaku merokok hanya dilakukan sekedarnya untuk menyenangkan perasaan.

c. Kenikmatan yang diperoleh dengan memegang rokok. Sangat spesifik pada perokok pipa. Perokok pipa akan menghabiskan waktu untuk mengisi pipa dengan tembakau sedangkan untuk menghisapnya hanya dibutuhkan waktu beberapa menit saja. Atau perokok lebih senang berlama-lama untuk memainkan rokoknya dengan jari-jarinya lama sebelum ia nyalakan dengan api.

2. Perilaku merokok yang dipengaruhi oleh perasaan negatif. Banyak orang yang menggunakan rokok untuk mengurangi perasaan negatif, misalnya bila ia marah, cemas, gelisah, rokok dianggap sebagai penyelamat. Mereka menggunakan rokok bila perasaan tidak enak terjadi, sehingga terhindar dari perasaan yang lebih tidak enak.

3. Perilaku merokok yang pecandu, mereka yang sudah pecandu akan menambah dosis rokok yang digunakan setiap saat setelah efek dari rokok yang dihisapnya berkurang. Mereka umumnya akan pergi keluar rumah membeli rokok, walau tengah malam sekalipun, karena ia khawatir kalau rokok tidak tersedia setiap saat ia menginginkannya.

4. Perilaku merokok yang sudah menjadi kebiasaan. Mereka menggunakan rokok sama sekali bukan karena untuk mengendalikan perasaan mereka, tetapi karena benar-benar sudah menjadi kebiasaannya rutin. Dapat dikatakan pada orang-orang tipe ini merokok sudah merupakan suatu perilaku yang bersifat otomatis, seringkali tanpa dipikirkan dan tanpa disadari. Ia menghidupkan api rokoknya bila rokok yang terdahulu telah benar-benar habis.

5. Bahaya Rokok

Rokok adalah benda beracun yang memberi efek santai dan sugesti merasa lebih jantan. Di balik kegunaan atau manfaat rokok yang secuil itu terkandung bahaya yang sangat besar bagi orang yang merokok maupun orang di sekitar perokok yang bukan perokok.

Ketika sebatang rokok terbakar terbentuklah 4.000 senyawa kimia, 200 diantaranya beracun dan 43 lagi pemicu kanker.

Efek racunnya terhadap sang perokok dibandingkan yang tidak merokok yaitu :

· 14x menderita kanker paru-paru, mulut, dan tenggorokan

· 4x menderita kanker esophagus

· 2x kanker kandung kemih

  • 2x serangan jantung

Rokok juga meningkatkan resiko kefatalan bagi penderita pneumonia dan gagal jantung, serta tekanan darah tinggi.

Asap rokok mengandung kurang lebih 4000 bahan kimia yang 200 diantaranya beracun dan 43 jenis lainnya dapat menyebabkan kanker bagi tubuh. Beberapa zat yang sangat berbahaya yaitu tar, nikotin, karbon monoksida, dsb.

2. Asap rokok yang baru mati di asbak mengandung tiga kali lipat bahan pemicu kanker di udara dan 50 kali mengandung bahan pengeiritasi mata dan pernapasan. Semakin pendek rokok semakin tinggi kadar racun yang siap melayang ke udara. Suatu tempat yang dipenuhi polusi asap rokok adalah tempat yang lebih berbahaya daripada polusi di jalanan raya yang macet.

3. Seseorang yang mencoba merokok biasanya akan ketagihan karena rokok bersifat candu yang sulit dilepaskan dalam kondisi apapun. Seorang perokok berat akan memilih merokok daripada makan jika uang yang dimilikinya terbatas.

4. Harga rokok yang mahal akan sangat memberatkan orang yang tergolong miskin, sehingga dana kesejahteraan dan kesehatan keluarganya sering dialihkan untuk membeli rokok. Rokok dengan merk terkenal biasanya dimiliki oleh perusahaan rokok asing yang berasal dari luar negeri, sehingga uang yang dibelanjakan perokok sebagaian akan lari ke luar negeri yang mengurangi devisa negara. Pabrik rokok yang mempekerjakan banyak buruh tidak akan mampu meningkatkan taraf hidup pegawainya, sehingga apabila pabrik rokok ditutup para buruh dapat dipekerjakan di tempat usaha lain yang lebih kreatif dan mendatangkan devisa.

5. Sebagian perokok biasanya akan mengajak orang lain yang belum merokok untuk merokok agar merasakan penderitaan yang sama dengannya, yaitu terjebak dalam ketagihan asap rokok yang jahat. Sebagian perokok juga ada yang secara sengaja merokok di tempat umum agar asap rokok yang dihembuskan dapat terhirup orang lain, sehingga orang lain akan terkena penyakit kanker.

6. Kegiatan yang merusak tubuh adalah perbuatan dosa, sehingga rokok dapat dikategorikan sebagai benda atau barang haram yang harus dihindari dan dijauhi sejauh mungkin. Ulama atau ahli agama yang merokok mungkin akan memiliki persepsi yang berbeda dalam hal ini.

6. Upaya Pencegahan

Dalam upaya prevensi, motivasi untuk menghentikan perilaku merokok penting untuk dipertimbangkan dan dikembangkan. Dengan menumbuhkan motivasi dalam diri untuk berhenti atau tidak mencoba untuk merokok, akan membuat mereka mampu untuk tidak terpengaruh oleh godaan merokok yang datang dari teman, media massa atau kebiasaan keluarga/orangtua.

Suatu program kampanye anti merokok yang dilakukan dapat dijadikan contoh dalam melakukan upaya pencegahan agar tidak merokok, karena ternyata program tersebut membawa hasil yang menggembirakan. Kampanye anti merokok ini dilakukan dengan cara membuat berbagai poster, film dan diskusi-diskusi tentang berbagai aspek yang berhubungan dengan merokok. Lahan yang digunakan untuk kampanye ini adalah sekolah-sekolah, televisi atau radio. Pesan-pesan yang disampaikan meliputi:

· Meskipun orang tuamu merokok, kamu tidak perlu harus meniru, karena kamu mempunyai akal yang dapat kamu pakai untuk membuat keputusan sendiri.

· Iklan-iklan merokok sebenarnya menjerumuskan orang. Sebaiknya kamu mulai belajar untuk tidak terpengaruh oleh iklan seperti itu.

· Kamu tidak harus ikut merokok hanya karena teman-temanmu merokok. Kamu bisa menolak ajakan mereka untuk ikut merokok.

Perilaku merokok akan memberikan dampak bagi kesehatan secara jangka pendek maupun jangka panjang yang nantinya akan ditanggung tidak saja oleh diri kamu sendiri tetapi juga akan dapat membebani orang lain (misal: orangtua)

7. Kesimpulan

Jadi dapat disimpulkan bahwa merokok merupakan kegiatan bodoh yang dilakukan manusia yang mengorbankan uang, kesehatan, kehidupan sosial, pahala, persepsi positif, dan lain sebagainya. Maka bersyukurlah anda jika belum merokok, karena anda adalah orang yang smart / pandai.

Ketika seseorang menawarkan rokok maka tolak dengan baik. Merasa kasihanlah pada mereka yang merokok. Jangan dengarkan mereka yang menganggap anda lebih rendah dari mereka jika tidak ikutan ngerokok. karena dalam hati dan pikiran mereka yang waras mereka ingin berhenti merokok.

Daftar pustaka